Tuteja Narendra, Ahmad Parvaiz, Panda Brahma B, Tuteja Renu
International Centre for Genetic Engineering and Biotechnology, Aruna Asaf Ali Marg, New Delhi 110067, India.
International Centre for Genetic Engineering and Biotechnology, Aruna Asaf Ali Marg, New Delhi 110067, India.
Mutat Res. 2009 Mar-Jun;681(2-3):134-149. doi: 10.1016/j.mrrev.2008.06.004. Epub 2008 Jul 3.
Plant cells are constantly exposed to environmental agents and endogenous processes that inflict damage to DNA and cause genotoxic stress, which can reduce plant genome stability, growth and productivity. Plants are most affected by solar UV-B radiation, which damage the DNA by inducing the formation of two main UV photoproducts such as cyclobutane pyrimidine dimers (CPDs) and pyrimidine (6-4) pyrimidone photoproducts (6-4PPs). Reactive oxygen species (ROS) are also generated extra- or intra-cellularly, which constitute yet another source of genotoxic stress. As a result of this stress, the cellular DNA-damage responses (DDR) are activated, which transiently arrest the cell cycle and allow cells to repair DNA before proceeding into mitosis. DDR requires the activation of Ataxia telangiectasia-mutated (ATM) and Rad3-related (ATR) genes, which regulate the cell cycle and transmit the damage signals to downstream effectors of cell-cycle progression. Since genomic protection and stability are fundamental to ensure and sustain plant diversity and productivity, therefore, repair of DNA damages is essential. In plants the bulky DNA lesions, CPDs and 6-4PPs, are repaired by a simple and error-free mechanism: photoreactivation, which is a light-dependent mechanism and requires CPD or 6-4PP specific photolyases. In addition to this direct repair process, the plants also have sophisticated light-independent general repair mechanisms, such as the nucleotide excision repair (NER) and base excision repair (BER). The completed plant genome sequences reveal that most of the genes involved in NER and BER are present in higher plants, which suggests that the network of in-built DNA-damage repair mechanisms is conserved. This article describes the insight underlying the DNA damage and repair pathways in plants. The comet assay to measure the DNA damage and the role of DNA repair helicases such as XPD and XPB are also covered.
植物细胞不断受到环境因素和内源性过程的影响，这些因素会对DNA造成损伤并引起基因毒性应激，从而降低植物基因组的稳定性、生长和生产力。植物受太阳UV-B辐射的影响最大，这种辐射通过诱导形成两种主要的紫外线光产物，如环丁烷嘧啶二聚体（CPD）和嘧啶（6-4）嘧啶酮光产物（6-4PPs）来损伤DNA。活性氧（ROS）也在细胞外或细胞内产生，这构成了另一种基因毒性应激源。由于这种应激，细胞的DNA损伤反应（DDR）被激活，它会暂时阻止细胞周期，并使细胞在进入有丝分裂之前修复DNA。DDR需要激活共济失调毛细血管扩张症突变（ATM）和Rad3相关（ATR）基因，这些基因调节细胞周期并将损伤信号传递给细胞周期进程的下游效应器。由于基因组保护和稳定性是确保和维持植物多样性及生产力的基础，因此，DNA损伤的修复至关重要。在植物中，大的DNA损伤，即CPD和6-4PPs，通过一种简单且无差错的机制进行修复：光复活作用，这是一种依赖光的机制，需要CPD或6-4PP特异性光解酶。除了这种直接修复过程外，植物还具有复杂的不依赖光的一般修复机制, 如核苷酸切除修复（NER）和碱基切除修复（BER）。完整的植物基因组序列表明，参与NER和BER的大多数基因存在于高等植物中，这表明内置的DNA损伤修复机制网络是保守的。本文描述了植物中DNA损伤和修复途径的潜在机制。还介绍了用于测量DNA损伤的彗星试验以及DNA修复解旋酶如XPD和XPB的作用。
